C-Jun N-terminal kinase (JNK) is a downstream signal of RhoB, which can directly upregulate the expression level of RhoB and/or increase the levels of GEF and ECT2 to increase the activity of RhoB, thereby phosphorylating JNK, triggering the pro-apoptotic protein Bim and leading to cell death; it has been speculated that there is a positive feedback relationship between them, with RhoB activity stimulating sustained JNK phosphorylation, thereby enhancing cervical cancer cell death through upregulation of RhoB (Chen et al., 2000) (Figure 5B). Here, ECT2 is linked to cervical carcinoma.